ReviewEpigenomics2026
Epigenetic regulation of non-coding DNA in placental development and disorders.
Review in Epigenomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human placenta is an epigenetically exceptional organ that must execute rapid proliferation, lineage bifurcation, and controlled invasion while maintaining immune tolerance at the maternal-fetal interface. Trophoblast lineages operate within a developmentally programmed "pseudo-malignant" regulatory state, characterized by global DNA hypomethylation, large partially methylated domains, and dynamic chromatin transitions across gestation. This configuration enables transcriptional plasticity but also creates vulnerability to maternal and environmental exposures, which can leave persistent epigenetic effects associated with fetal growth restriction, preeclampsia, preterm birth, and pregnancy loss. Placental health and disease therefore cannot be understood through protein-coding genes alone. The non-coding genome, comprising promoters, enhancers, enhancer-promoter networks, and non-coding RNAs is extensively rewired in trophoblast, with retrotransposons providing a major source of regulatory innovation. Epigenetic mechanisms coordinate these elements to establish trophoblast-specific transcriptional programs, and perturbation at any layer can disrupt differentiation, invasion, endocrine signaling, and immune modulation. Maternal inflammation, hypoxia, toxins, metabolic and psychological stress reshape epigenetically labile non-coding regions, positioning the placenta as both a developmental sensor and molecular archive of the intrauterine environment. Advances in epigenomic profiling highlight the potential of non-coding epigenetic signatures as early biomarkers, while underscoring ongoing challenges in resolving cell-type-specific regulatory programs and accurately annotating repetitive elements.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.